Humans have independent senses of movement and positron of the limbs. In this study, which is part of an ongoing series of studies to investigate the neural mechanisms of proprioception, we seek to discover the neural substrate providing limb positron information and, ultimately , to determine how this information is used in the control of movement. The study will focus first on how positron of a joint is coded by static- positron mechanisms, that is, mechanisms that can function when the joints are stationary. Such mechanisms must rely on continuously available, though not necessarily ongoing, sensory from receptors in muscles, likely the muscle spindles that measure muscle length. However, spindles in relaxed humans respond far too weakly to account for the accuracy people display in judging joint positron. We will test the hypothesis that the nervous system derives an accurate measure of absolute positron of a joint by enhancing the sensitivity of the spindles with fusimotor activation when positron determination is needed. Static-positron sense will be tested in humans under a variety of normal conditions and during partial local anesthetic block of muscle nerves intended to prevent fusimotor activation of the spindles without substantially affecting transmission of positron signals from the spindles. A deficit in static-positron sense caused by a partial block would provide evidence that fusimotor activation is necessary for static- positron sense and would also argue for the possibility of independent control of alpha and gamma motor activity. The study next focuses on how positron can be encoded by movement mechanisms. The nervous system appears to derive joint positron mainly from movement signals probably because this derivation is faster than obtaining positron from the static-positron mechanism. However, positron derived from velocity signals dose not yield absolute or baseline positron but only a measure of change in positron. We will test whether information about joint positron derived from movement signals doses fall to provide a sense of absolute positron as predicted. Finally we will test the hypothesis that movement signals from which positron is derived come from muscle receptors only and not from skin/or joint receptors.